This is a continuation-in-part of copending application Ser. No. 921,823, filed Oct. 21, 1986, now abandoned which is a continuation of Ser. No. 834,129 filed Feb. 26, 1986, now abandoned, which in turn is a continuation of Ser. No. 506,824, filed June 23, 1983, now abandoned, whose entire contents are hereby incorporated by reference.
This invention relates to tobacco smoking articles and their construction, and also to methods for reducing the health risks of smokers.
It is known that tobacco and, more particularly, tobacco smoke contain numerous potential carcinogens and cocarcinogens. Accounts of Chem. Res., S. Hecht et al, 12: 92-98 (1979). Cancer Research, D. McCoy et al, 41, 2849-2854 (1981). Some of these potential carcinogens and cocarcinogens are tobacco specific; that is, they are associated with and are introduced only by the use of tobacco. It is also known that N'-Nitrosonoronicotine (NNN) is one of the major tobacco-specific carcinogens occurring in tobacco and also in the particulate phase of tobacco smoke. N-Nitroso Compounds in the Environment: IARC Scientific Publication. No. 9, pp. 159-165, D. Hoffmann et al (1975). See also, Studies on the Reduction of Nitrosamines in Tobacco, W.J. Chamberlain et al, Tobacco Science 81 (1981). ("It is known that N-nitroso derivatives of tobacco alkaloids, such as N,nitrosornicotine (NNN) and 4-N-methyl-N-nitrosamino)-1-(3-pyridyo-1-butano (NNK) are powerful environmental carcinogens.").
Other related nitrosamines such as N-Nitrosopyrrolidine (NPYR) are found in cooked bacon and other processed meats, as well as in tobacco and tobacco smoke. IARC Science Publication, D. Harvery et al, 17: 313 (1978). Hence, nitrosamines can arrive in the environment from several sources.
Recent experimentations with NNN have left little doubt that this compound is likely to be a potent carcinogen or precarcinogen in mammals. By administering NNN in drinking water, esophageal tumors have been induced in F-344 rats. Carcinogenesis. S. Hecht et al, 3: 453-456 (1982). Further, administration of NNN is also known to induce carcinogenesis in the olfactory epithelium, lung, salivary glands of rodents. See Cancer Research, W. Waddell et al, 40: 3518-3523 (1980). Moreover, the presence of a metabolite of NNN at the sites of tumor formation has been confirmed by radio labelling experiments. A whole-body autoradiography study of adult male C57BL/6J mice, utilizing [.sup.14 C] NNN to assess the specific distribution of NNN and its metabolites in all the tissues of the body, revealed a striking correlation of the retention of radioactivity with the previously reported sites of tumor formation Cancer Research, W. Waddell et al, 40: 3518-3523 (1980).
It has interestingly been discovered that NNN exhibits an extraordinary degree of selection in inducing tumor formation. That is, NNN typically induces tumor formation at five sites, namely the nasal cavity, salivary duct, esophagus, bronchial epithelium and the liver, Cancer Research, supra. While the precise method of NNN carcinogenesis is unclear, there is evidence that the proximal carcinogen is formed following the a -hydroxylation of NNN in vivo. Cancer Research, C. Chen et al, 38: 3639-3645 (1978). Cancer Research, W. Waddell et al, 40: 3518-3523 (1980). Experimentation has indicated, for example, that the F-344 rat esophagus, in contrast to other tissues, preferentially catalyzes hydroxylation at the a-carbon of NNN adjacent to the pyridine ring. Carcinogenesis, S. Hecht et al, 3: 453-456 (1982). Thus, the selective retention of NNN and metabolites thereof in sites where tumor formations are known to occur preferentially allows an excellent correlation of molecular accumulation with carcinogenic activity. However, despite the increasingly strong nexus between the tumor incidence, reactive nitrosamines such as NNN continue to be ubiquitous in the environment, especially including in the tobacco smoke stream.
A number of proposals have been made to reduce the amount of such substances inhaled by the smoker in the smoke stream. Generally, these proposals fall into three categories. The first category pertains to methods for reducing the irritant material itself, generally through changes in tobacco blends, by special growing, processing or extraction, by the partial or total replacement of the tobacco with tobacco substitutes, or by varying the tobacco's combustion temperatures. The second category is concerned with the dilution of the smoke before it enters the smoker's mouth, as for example by the use of highly permeable cigarette paper or filter paper or by the perforation of the cigarette filter to allow air to be drawn directly into the smoke stream. The third category of proposals deals with the construction of the filter itself to achieve the high filtration or the selective removal of particulate matter.
While many of these proposals, individually or in combination have been successfully commercialized, each reduction of the tar and nicotine yield and of irritating substances is accompanied by a corresponding reduced level of the resulting smoker satisfaction. Further, although many substances have been isolated as carcinogenic, gross reduction of tar and nicotine yields and gross reduction of irritating substances does not selectively reduce the isolated carcinogen because these proposals do not selectively or effectively isolate these carcinogens. Recent sales data indicate that, despite various products purporting unique methods of maintaining taste satisfaction at reduced levels of tar and nicotine and irritant deliveries, sales of lowered tar and nicotine and irritant products, particularly those commercially classified as "ultra low tar and nicotine" products, are decreasing. Further in accordance with the preceding, the practical deficiency of products purporting to selectively or grossly remove substantially all of an isolated carcinogenic material is evidenced by recent data which indicates that long-term cancer incidences have not, as one would have expected from the adoption of such products, been reduced but, rather, have increased. Additionally, no known cigarette or cigarette filter designs preferentially reduces or filters out any chemical compound, in particular, any carcinogen. Known cigarettes and cigarette filters also do not discriminate as to particulate matter or carcinogens.
Clearly then, the practice of reducing either tar and nicotine and irritant content or reducing specific carcinogenic matter content is severely limited in terms of the efficacy thereof for reducing irritants to which a smoker is exposed or for reducing the smoker's continued exposure to the health risks associated with carcinogenic matter found in the smoke stream. This is evidenced by the smoker's dissatisfaction with ultra low levels of tar and nicotines due to unacceptable low taste satisfaction. It is further accepted that mere gross reductions in smoke stream constituents at the very least fails to reduce the isolated carcinogens below a concentration in the smoke stream that would be non-toxic, and, in the case of eliminating isolated carcinogens, is a deficient course of action.